Page 242 - Small Animal Clinical Nutrition 5th Edition

Food Safety 245

The dog was hospitalized for 20 days. Additional therapies administered included famotidine (0.5 mg/kg IV q12hours) to min-
imize gastric hyperacidity, cefazolin (22 mg/kg IV q8hours) for prophylaxis to prevent infection from the peritoneal dialysis
VetBooks.ir catheters and total parenteral nutrition, which was administered for seven days, at which time the dog began to eat on its own. A

biochemistry profile performed at the time of discharge revealed these values: urea nitrogen 52 mg/dl, creatinine 3.0 mg/dl and
phosphorous 11.5 mg/dl.
Because of the previously diagnosed idiopathic hyperlipidemia, a diet change was not initiated in this dog. A chitin-based phos-
b
phate binder (Epakitin ) was added to the food to control hyperphosphatemia. The higher protein content of the food (vs. foods
formulated for renal failure) necessitated three to four times the standard dose of phosphate binder to control hyperphosphatemia.
There was also a concern that the increased protein in the food would increase intraglomerular pressure; therefore, the dog was given
enalapril (0.25 mg/kg PO q24hours). At four months from discharge, the dog had a stable creatinine at 3.7 mg/dl, phosphorous of
6.0 mg/dl and was reported to be active and eating well.

Endnotes
a. Hill’s Pet Nutrition, Inc., Topeka, KS, USA.
b. Vetoquinol, Buena, NJ, USA.

CASE 11-5

Acute Vomiting in a German Shepherd Dog
Kiko Bracker, DVM, Dipl. ACVECC
Angell Animal Medical Center
Boston, Massachusetts, USA

Patient Assessment
A nine-year-old, neutered male, German shepherd dog was examined for a three-day history of occasional vomiting and progres-
sive lethargy. The dog was uninterested in food for the past few days and was drinking excessively. Before the onset of these signs,
the dog had been healthy and no medications had been administered.
Physical examination revealed a 46-kg dog with a normal body condition score (5/9 [BCS]). Vital signs were within normal lim-
its. The dog was lethargic, but responsive and able to walk around the exam room. The abdomen was not painful and abdominal
palpation was normal.The mucous membranes were tacky and faintly icteric, as were the sclera.Thoracic auscultation was normal.
Diagnostic evaluation included a complete blood count, which showed hemoconcentration (hematocrit = 55%), and a serum bio-
chemistry panel, which revealed hyperbilirubinemia and increased liver enzyme activities (Table 1). A coagulogram showed that the
prothrombin time (PT) and activated partial thromboplastin time (aPTT) were prolonged (Table 1). Results of a urinalysis were
normal except for bilirubinuria.
Abdominal radiography showed no significant abnormalities. An abdominal ultrasound found the gallbladder to be full, but
showed no dilatation of the bile ducts. The liver appeared structurally normal although a small amount of fluid was noted between
the liver lobes that could not be sampled due to its location. Because of the prolonged clotting times and concern of bleeding, no
liver biopsy or aspirates were taken. The tentative diagnosis was an acute hepatic insult of unknown cause.

Assess the Food and Feeding Method
The dog had been eating the same brand of dry dog food for several years.The exact daily caloric intake was unknown because the
dog was fed free choice. Upon further questioning, the owner admitted the dog had been eating a food that was identified as being
contaminated with aflatoxin. Based on national recall information, a primary rule out of aflatoxin toxicosis was established.
Questions
1. What method of delivering nutrition to this patient is most appropriate during its hospitalization?
2. How can a diagnosis of aflatoxicosis be confirmed?
3. Is there a specific antidote for this toxin?